ABSTRACT The aim of the study was the evaluation of risperidone effect on metabolite measures in the frontal lobe, temporal lobe and thalamus in schizophrenic patients on the basis of proton magnetic resonance spectroscopy ( (1)H MRS).
A group of 14 patients with the diagnosis of schizophrenia, according to DSM-IV, were examined in the study. The patients were examined twice, once after a period of at least 7 days without neuroleptics and for the second time at least 4 weeks after stable risperidone doses.
The significant differences in the metabolite levels before and after the treatment were observed only in thalamus: an increase in myoinositol (mI) and N-acetylaspartate (NAA) levels. Positive symptoms before the treatment correlated positively with NAA level in the frontal lobes and negatively in the temporal lobes. Negative symptoms before the treatment correlated positively with Glx (a common signal for GABA, glutamine and glutamate) level in the temporal lobes.
Our results seem to confirm the influence of risperidone on the brain metabolism, specifically in the region of thalamus.

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Behavioral and cognitive dysfunction, particularly social and communication impairments, are shared between autism and schizophrenia spectrum disorders, while evidence for a diametric autism-positive schizophrenia symptom profile is inconsistent. We investigated the shared phenotype at a personality trait level, particularly its resemblance to schizoid per-sonality disorder, as well as differential aspects of the autism–schizophrenia model. Items of the autism spectrum quotient (AQ) and schizotypal personality questionnaire (SPQ) were pseudo-randomly combined, and were completed by 449 (162 male, 287 female) non-clinical participants aged 18–40. A factor analysis revealed three factors; the first repre-sented a shared social disorganization phenotype, the second reflected perceptual oddities specific to schizotypy while the third reflected social rigidity specific to autism. The AQ and SPQ were strongly correlated with Factor 1 (AQ: r = 0.75, p < 0.001; SPQ: r = 0.96, p < 0.001), SPQ score was correlated with Factor 2 (r = 0.51, p < 0.001), particularly in cognitive–perceptual features (r = 0.66, p < 0.001), and AQ score was strongly correlated with Factor 3 (r = 0.76, p < 0.001). Furthermore, there was no relationship between Factor 1 and Factor 2.Thus, there is robust evidence for a shared social disorganization phenotype in autistic and schizotypal tendency, which reflects the schizoid phenotype. Discriminating and independent dimensions of schizotypal and autistic tendency exist in Factors 2 and 3, respectively. Current diagnostic protocols could result in different diagnoses depending on the instrument used, suggesting the need for neuromarkers that objectively differentiate autistic and schizotypal traits and resolve the question of commonality versus co-morbidity.

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Schizophrenia is characterized by loss of brain volume, which may represent an ongoing pathophysiological process. This loss of brain volume may be explained by reduced neuropil rather than neuronal loss, suggesting abnormal synaptic plasticity and cortical microcircuitry. A possible mechanism is hypofunction of the NMDA-type of glutamate receptor, which reduces the excitation of inhibitory GABAergic interneurons, resulting in a disinhibition of glutamatergic pyramidal neurons. Disinhibition of pyramidal cells may result in excessive stimulation by glutamate, which in turn could cause neuronal damage or death through excitotoxicity.
In this study, GABA/creatine ratios, and glutamate, NAA, creatine and choline concentrations in the prefrontal and parieto-occipital cortices were measured in 17 patients with schizophrenia and 23 healthy controls using proton magnetic resonance spectroscopy at an ultra-high magnetic field strength of 7 T. Significantly lower GABA/Cr ratios were found in patients with schizophrenia in the prefrontal cortex as compared to healthy controls, with GABA/Cr ratios inversely correlated with cognitive functioning in the patients. No significant change in the GABA/Cr ratio was found between patients and controls in the parieto-occipital cortex, nor were levels of glutamate, NAA, creatine, and choline differed in patients and controls in the prefrontal and parieto-occipital cortices. Our findings support a mechanism involving altered GABA levels distinguished from glutamate levels in the medial prefrontal cortex in schizophrenia, particularly in high functioning patients. A (compensatory) role for GABA through altered inhibitory neurotransmission in the prefrontal cortex may be ongoing in (higher functioning) patients with schizophrenia.

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The amino-acid N-acetyl-aspartate (NAA) is located in neurons and the concentration of NAA correlates with neuronal mitochondrial function. The signal of NAA, as measured with proton magnetic resonance spectroscopy (1H-MRS), is considered to reflect both, neuronal density and integrity of neuronal mitochondria. A reduction of the NAA concentrations has been found in several psychiatric disorders. Newer studies report reversal of decreased NAA concentration with treatment. The objective of this review is to summarize the literature on NAA changes in association with psychopharmacological treatment in psychiatric disorders (affective disorders, obsessive-compulsive disorder, schizophrenia and dementia).
The majority of studies identified increased NAA concentrations in response to treatment, while a smaller number of studies did not find this effect. The NAA increase seems to be neither specific for a certain disorder nor for a specific intervention. This suggests that the reduction of NAA may represent an altered functional (metabolic) state of neurons common to different psychiatric disorders and the increase after treatment to indicate functional restoration as one general effect of interventions.

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